cholecalciferol and fasudil

Cerebral cavernous malformations (CCMs) are ectatic capillary-venous malformations that develop in approximately 0.5% of the population. Patients with CCMs may develop headaches, focal neurologic deficits, seizures, and hemorrhages. While symptomatic CCMs, depending upon the anatomic location, can be surgically removed, there is currently no pharmaceutical therapy to treat CCMs. Several mouse models have been developed to better understand CCM pathogenesis and test therapeutics. The most common mouse models induce a large CCM burden that is anatomically restricted to the cerebellum and contributes to lethality in the early days of life. These inducible models thus have a relatively short period for drug administration. We developed an inducible CCM3 mouse model that develops CCMs after weaning and provides a longer period for potential therapeutic intervention. Using this new model, three recently proposed CCM therapies, fasudil, tempol, vitamin D

Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Acute Disease; Animals; Apoptosis Regulatory Proteins; Brain; Cholecalciferol; Chronic Disease; Cyclic N-Oxides; Disease Models, Animal; Gene Deletion; Hemangioma, Cavernous, Central Nervous System; Hemorrhage; Lipopolysaccharides; Mice, Inbred C57BL; Models, Biological; Phenotype; Spin Labels